TY - JOUR. T1 - Monoclonal antibody to a nucleolar antigen of human B-lymphoblastoid cells. AU - Todorov, I. T.. AU - Philipova, R. N.. AU - Zhelev, N. Z.. AU - Hadjiolov, A. A.. PY - 1987/3. Y1 - 1987/3. N2 - An anti-nucleolar monoclonal antibody reacting with human B-lymphoblastoid cells but not with normal periferal blood lymphocytes has been isolated. The antibody recognized in Namalwa cells an antigen with molecular mass 41 kDa and pI 5.6, different from all previously described nucleolar antigens. Inhibition of rRNA transcription with Actinomycin D caused redistribution of the 41 5.6 antigen, but even at long term drug action it remains associated with the nucleolar remnants.. AB - An anti-nucleolar monoclonal antibody reacting with human B-lymphoblastoid cells but not with normal periferal blood lymphocytes has been isolated. The antibody recognized in Namalwa cells an antigen with molecular mass 41 kDa and pI 5.6, different from all previously described nucleolar antigens. Inhibition of ...
TY - JOUR. T1 - Direct effects of HP Acthar Gel® on human B lymphocyte activation in vitro. AU - Olsen, Nancy. AU - Decker, Dima A.. AU - Higgins, Paul. AU - Becker, Patrice M.. AU - McAloose, Carl A.. AU - Benko, Ann L.. AU - Kovacs, William. PY - 2015/10/27. Y1 - 2015/10/27. N2 - Introduction: Both clinical experience and experimental evidence have suggested that Adrenocorticotropic hormone (ACTH) might directly exert immunomodulatory effects not dependent on adrenal steroidogenesis. Methods: The direct effects of H.P. Acthar Gel® (Acthar), a repository preparation containing a porcine ACTH analogue, on human B lymphocyte function were studied in vitro using peripheral blood B cells isolated using anti-CD19 coated magnetic beads and activated by interleukin 4 (IL-4) and CD40 ligand (CD40L). Analysis of expression of messenger RNA (mRNA) encoding activation-induced cytidine deaminase (AICDA) was carried out by quantitative real-time polymerase chain reaction (PCR). Cellular proliferation was ...
TY - JOUR. T1 - CXCR5-dependent entry of CD8 T cells into rhesus macaque B-cell follicles achieved through T-cell engineering. AU - Ayala, Victor I.. AU - Deleage, Claire. AU - Trivett, Matthew T.. AU - Jain, Sumiti. AU - Coren, Lori V.. AU - Breed, Matthew W.. AU - Kramer, Joshua A.. AU - Thomas, James A.. AU - Estes, Jacob. AU - Lifson, Jeffrey D.. AU - Ott, David E.. PY - 2017/6/1. Y1 - 2017/6/1. N2 - Follicular helper CD4 T cells, TFH, residing in B-cell follicles within secondary lymphoid tissues, are readily infected by AIDS viruses and are a major source of persistent virus despite relative control of viral replication. This persistence is due at least in part to a relative exclusion of effective antiviral CD8 T cells from B-cell follicles. To determine whether CD8 T cells could be engineered to enter B-cell follicles, we genetically modified unselected CD8 T cells to express CXC chemokine receptor 5 (CXCR5), the chemokine receptor implicated in cellular entry into B-cell follicles. ...
The VH gene repertoire of human peripheral B cells was analyzed using PCR analysis of individual blood B cells. Because genomic DNA of single B cells was analyzed, data from both productive and nonproductive VDJ rearrangements were obtained. Nine out of 75 B cells contained both functional and nonfunctional rearrangement products, whereas 62/75 had a single productive VDJ rearrangement. The distribution of VH families was ordered in accordance with the germline complexity, although a bias toward VH3 and some of its members was found. This bias was noted in both the productively and nonproductively rearranged repertoires, indicating that it resulted from molecular and not selective processes. Evidence for negative selection of certain VH3 and VH4 family members was noted in that they were found less often as productive than nonproductive VDJ rearrangements. In addition, evidence for positive selection based on CDR3 was obtained, in that JH6 and DXP1 were found at a higher frequency in the ...
Brezinschek, H.P., Brezinschek, R.I. & Lipsky, P.E., 1995, Analysis of the Heavy Chain Repertoire of Human Peripheral B Cells Using Single-Cell Polymerase Chain Reaction, Journal of Immunology, 155:191-202 ...
Background. High serum levels and enhanced in vitro production of IgA are observed in more than half of patients with IgA nephropathy (IgAN); and transforming forming growth factor‐β (TGF‐β) is certain IgA class switching factor. On the other hand, macroscopic haematuria appears frequently with upper respiratory infection as tonsillitis in IgAN.. Methods. We compared the lymphocytic response to in‐vitro stimulation by group A streptococcal M proteins of apparent virulence factor between IgAN, non‐proliferative glomerulonephritis (NPGN), and normal subjects. M proteins were extracted from group A streptococcal strain type 5 and type 12 determined serologically.. Results. M protein‐induced proliferation of lymphocytes from IgAN was higher than in NPGN but not in healthy control subjects. Flow cytometric analysis indicated that stimulation by M protein extracts derived from type 5 streptococci (M5) increased surface IgA‐positive B cells in IgAN, but did not activate the production of ...
TY - JOUR. T1 - The role of B cell proliferation in the generation of immunoglobulin-secreting cells in man. AU - Jelinek, Diane F. AU - Lipsky, P. E.. PY - 1983. Y1 - 1983. N2 - The relationship of B cell proliferation and the generation of immunoglobulin-secreting cells (ISC) was explored in vitro by examining the effect of hydroxyurea (HU), an inhibitor of cellular DNA synthesis, on the generation of ISC from human peripheral blood mononuclear cells (PBM). HU completely inhibited the capacity of PBM to generate ISC in response to pokeweed mitogen (PWM) and other polyclonal B cell activators. Inhibition resulted from an effect on B cell proliferation, because HU also prevented the generation of ISC in cultures of purified B cells supplemented with either T cell supernatants or mitomycin C-treated T cells. Inhibiting B cell proliferation by treating them with mitomycin C before culture also abolished the generation of ISC. When ISC were enumerated after a 7-day incubation with PWM, the addition ...
Results Twenty patients were included. Nine were treated by etanercept (ETN), 9 by certolizumab pegol and 2 by adalimumab. The percentage of B cells significantly increased under TNFi from (median [IQR 25-75]) 4.6 (3.5-6.7) to 7.6 (5.2-9.9) % of lymphocytes. No change was observed in the different subtypes of B cells. However, in patients treated with ETN, IgD-CD27- double negative memory B cells significantly increased from 4.6 (2.5-5.4) to 7.7 (6.2-11.0)(p=0.03). The variation of those double negative B cells were significantly different from those observed with monoclonal antibodies (+1.6 [0.0-5.4] vs 0.3 [-1.3-1.8]% of B cells, p=0.02). No change of T, NK, NKT cells was observed in either group. EULAR responders at 3 months had significantly higher percentage of CD27+ memory B cells at baseline (32.9 [25.2-40.6] vs 19.5 [12.3-19.6]% of B cells, respectively; p=0.02), especially IgD+CD27+ pre-switch memory B cells (19.3 [9.8-21.8] vs 5.9 [4.9-9.4]% of B cells, respectively; p=0.02). Since ...
Interleukin 10 (IL-10) is a pleiotropic factor that enhances proliferation of activated human B lymphocytes and induces them to secrete high amounts of immunoglobulins. Here we show that several human B cell lines were able to constitutively secrete human (h)IL-10. Whereas none of the pre-B nor the plasmocytic cell lines tested produced hIL-10, 25 of the 36 tested mature B cell lines (lymphoblastoid and Burkitt lymphoma cell lines) secreted hIL-10. Moreover, 24 of these 25 hIL-10-producing B cell lines contained the Epstein-Barr virus (EBV) genome, suggesting a relationship between hIL-10 production by human B cell lines and EBV expression. Accordingly, whereas polyclonal activation via triggering of surface immunoglobulins or CD40 antigen induced highly purified normal human B lymphocytes to produce only low (0.3-0.4 ng/ml) but significant amounts of hIL-10, EBV infection induced them to secrete high amounts of hIL-10 (4-9 ng/ml). Furthermore, addition of exogenous hIL-10, simultaneously to EBV ...
TY - JOUR. T1 - Anti-nuclear antibody reactivity in lupus may be partly hard-wired into the primary B-cell repertoire. AU - Chang, Sooghee. AU - Yang, Liu. AU - Moon, Young Mee. AU - Cho, Young Gyu. AU - Min, So Youn. AU - Kim, Tae Joo. AU - Kim, Young Joo. AU - Patrick, Wilson. AU - Kim, Ho Youn. AU - Mohan, Chandra. PY - 2009/10. Y1 - 2009/10. N2 - When monoclonal ANAs and non-ANAs generated from a genetically simplified mouse model of lupus, B6.Sle1, were recently compared, the ANAs exhibited three sequence motifs in their immunoglobulin heavy chains, including increased cationicity in CDR3 (motif A), reduced anionicity in CDR2 (motif B) and increased aspartate at H50 (motif C). The present study was designed to elucidate the extent to which these ANA-associated sequence motifs might be hard-wired into the primary B-cell repertoire in lupus. The immunoglobulin heavy chain sequence of total splenic B-cells, follicular B-cells and marginal zone B-cells from B6.Sle1 congenic mice and ...
We have been trying to get some MAIDS B cell tumors to grow in B6 mice. The tumors originally came from B6 mice but have been grown in tissue culture for several years. In the event we can not readapt them to grow in vivo we are in need of other tumors. If anyone has a B cell tumor, preferably before the plasma cell stage, and after the immature B cell stage that they have grown in B6 mice we would appreciate hearing about it. If it also grows in tissue culture, while being readly passed back into mice that would be a bonus. Please repond to this service or my email address:wiliam.wade at dartmouth.edu Thanks for your attention and help in this matter. Sincerely, William F. Wade, Ph.D. Assistant Professor of Microbiology Dartmouth Medical School ...
Schlegel, R A.; Von boehmer, H; and Shortman, K, Antigen-initiated b lymphocyte differentiation. V. Electrophoretic separation of different subpopulations of afc progenitors for unprimed igm and memory igg responses to the nip determinant. (1975). Subject Strain Bibliography 1975. 1320 ...
CURRENT PROJECTS: - Using mouse genetics to identify the susceptibility factors that control B cell tolerance, differentiation and survival, leading to autoantibody production. - Defining the mechanisms by which autoimmune susceptibility elicits inflammation and recruitment of innate immune cells in secondary lymphoid organs that affect B cell function. - Examining helper activity and inflammatory cytokines of human T cells in peripheral blood of SLE patients that affect B cell function. - Characterizing the regulation and activity in primary mouse T follicular helper cells and T follicular regulatory cells to control B cell responses. - Defining the signal transduction events through the BCMA cytokine receptor that regulates both T follicular helper cell homeostasis and plasma cell survival in autoimmunity. - Characterizing the development and persistence of IgE antibodies to airway allergens. Go to Loren Ericksons Lab Site for detailed information about his lab and his research ...
Nonhomologous end-joining (NHEJ) repairs DNA double-strand breaks (DSBs) during V(D)J recombination in developing lymphocytes and during immunoglobulin (Ig) heavy chain (IgH) class switch recombination (CSR) in peripheral B lymphocytes. We now show that CD21-cre-mediated deletion of the Xrcc4 NHEJ gene in p53-deficient peripheral B cells leads to recurrent surface Ig-negative B lymphomas (CXP lymphomas). Remarkably, CXP lymphomas arise from peripheral B cells that had attempted both receptor editing (secondary V[D]J recombination of Igκ and Igλ light chain genes) and IgH CSR subsequent to Xrcc4 deletion. Correspondingly, CXP tumors frequently harbored a CSR-based reciprocal chromosomal translocation that fused IgH to c-myc, as well as large chromosomal deletions or translocations involving Igκ or Igλ, with the latter fusing Igλ to oncogenes or to IgH. Our findings reveal peripheral B cells that have undergone both editing and CSR and show them to be common progenitors of CXP tumors. Our ...
Fingerprint Dive into the research topics of An EBV-transformed owl monkey B-lymphocyte cell line.. Together they form a unique fingerprint. ...
TY - JOUR. T1 - The CD40 ligand expressed by human B cells costimulates B cell responses. AU - Grammer, A. C.. AU - Bergman, M. C.. AU - Miura, Y.. AU - Fujita, K.. AU - Davis, L. S.. AU - Lipsky, P. E.. PY - 1995/1/1. Y1 - 1995/1/1. N2 - The possibility that activated B cells might express a ligand for CD40 that was of functional importance for B cell responses was examined by using highly purified human peripheral blood B cells, as well as a variety of B lymphoblastoid cell lines and hybridomas. Following stimulation with the combination of a calcium ionophore and a phorbol ester, human B cells bound a soluble fusion protein containing the extracellular portion of CD40 and the Fc region of lgG1 (CD40.lg). A variety of B cell lines and hybridomas also bound CD40.1g, either constitutively or after activation. In addition, CD40.Ig specifically immunoprecipitated a 33-kDa glycoprotein from surface 125I-labeled activated B cells. The nucleotide sequence of the coding region of the CD40 ligand mRNA ...
B cells play a central role in immune system function. Deregulation of normal B cell maturation can lead to the development of autoimmune syndromes as well as B cell malignancies. Elucidation of the molecular features of normal B cell development is important for the development of new target therapies for autoimmune diseases and B cell malignancies. Employing B cell-specific conditional knockout mice, we have demonstrated here that the transcription factor leukemia/lymphoma-related factor (LRF) forms an obligate dimer in B cells and regulates mature B cell lineage fate and humoral immune responses via distinctive mechanisms. Moreover, LRF inactivation in transformed B cells attenuated their growth rate. These studies identify what we believe to be a new key factor for mature B cell development and provide a rationale for targeting LRF dimers for the treatment of autoimmune diseases and B cell malignancies.. ...
The growth and differentiation of B cells to immunoglobulin (Ig)-secreting cells is regulated by a variety of soluble factors. This study presents data that support a role for transforming growth factor (TGF)-beta in this regulatory process. B lymphocytes were shown to have high-affinity receptors for TGF-beta that were increased fivefold to sixfold after in vitro activation. The addition of picogram quantities of TGF-beta to B cell cultures suppressed factor-dependent, interleukin 2 (IL 2) B cell proliferation and markedly suppressed factor-dependent (IL 2 or B cell differentiation factor) B cell Ig secretion. In contrast, the constitutive IgG production by an Epstein Barr virus-transformed B cell line was not modified by the presence of TGF-beta in culture. This cell line was found to lack high-affinity TGF-beta receptors. The degree of inhibition of B cell proliferation observed in in vitro cultures was found to be dependent not only on the concentration of TGF-beta added but also on the ...
Mice with the autosomal recessive severe combined immune deficiency (scid) mutation lack mature lymphocytes because of defective joining of T cell receptor and immunoglobulin (Ig) gene segments. Penetrance of this mutation is incomplete since 10-25% of SCID mice produce some T or B lymphocytes. This leaky phenotype could be due to a reversion of the mutation in some mice or to a constant, low frequency of functional lymphocytes generated in all SCID mice with variable survival of such cells. We report here that all SCID mice can be stimulated to produce functional B cells by the transfer of normal neonatal, but not adult, T cells. T cell-induced rescue of C.B-17scid B cells results in high levels of Ig expressing the Ighb allotype of the SCID recipient. These results show that all SCID mice generate some functional B cells, the majority of which do not survive in the absence of a subset of T cells present in high frequency in the neonate ...
To order B-Lymphocyte Activation Antigen B7-2 (LAB7-2) Polyclonal Antibody , please use the Cat. Nr. CAU27021 and submit your purchase order by email or by fax. A discount is available for larger or bulk quantities, please contact us for more information ...
Intercellular adhesion molecule (ICAM) 1/CD54 plays an important role in T cell dependent B cell activation and for function of B lymphocytes as antigen-presenting cells. ICAM-1 expression is upregulated as a consequence of B lymphocyte antigen receptor (BCR) signaling, thereby serving to render antigen-stimulated B cells more receptive to T cell-mediated costimulatory signals. We have investigated BCR-induced expression of the Icam-1 gene in primary B cells and B cell lines and have found it to be dependent on BCR-induced expression of the transcription factor EGR1. Icam-1 transcription, induced by BCR cross-linking or bypassing the BCR with phorbol ester, is absent in a B cell line in which the EGR1-encoding gene (egr-1) is methylated and not expressed. A potential EGR1-binding site was located at -701 bp upstream of the murine Icam-1 gene transcription start site and shown by electrophoretic mobility shift assay to bind to murine EGR1. Mutation of this site in the context of 1.1 kb of the ...
Etiologic-based therapy is an ideal pharmacological option to treat or prevent diseases. There is no known etiology for multiple sclerosis (MS); however, envir...
Brown, L D.; Shen, F W.; Uhr, J W.; and Vitetta, E S., The expression of lyb-2.1 On murine b lymphocytes. Abstr. (1978). Subject Strain Bibliography 1978. 1222 ...
After infection with progressed mechanisms to escape a protective B cell response by inducing a strong polyclonal B cell activation (7, 8), B cell anergy (9), and apoptosis (10). Presumably, successful rearrangement of the H chain and a correctly assembled pre-BCR allow pre-B II cells to proliferate (15). After rearrangement of the L chain locus, pre-B II cells become immature B cells leave the bone marrow at the transitional B cell stage and complete their final development into mature B cells in the periphery (16). Bone marrow stromal cells are essential components of the hematopoietic microenvironment and are absolutely required for the maintenance of hemotopoietic stem cells (17) and the development of B cells (18). Stromal cells form a network in the inter-sinusoidal spaces of the bone cavity that extends from the endosteum to the endothelial cell basement membrane of the sinusoids (19). The interstitia of this network support the growth and differentiation of B cells in close contact with ...
Intraocular lymphoma is an aggressive non-Hodgkin B cell lymphoma involving the posterior eye. Basic research on this tumour has been hindered by an inability to expand the malignant B cell population. We developed a cell culture system, in which endothelial cell monolayers were infected with adenoviral vectors encoding HIV-1 proteins, Vpu and Tat. These monolayers permitted adhesion and proliferation of CD20-positive B cells from specimens of cerebrospinal fluid obtained from patients with intracranial tumor. The system provides a method for expansion of the malignant B cell population present in small volumes of fluid that are available for research use. ...
New insights into human B cell biology. B cells are highly important white blood cells known as lymphocytes and are part of the adaptive immune system. B cells have a specialised receptor on their cell surface (B cell receptor, BCR) which recognises specific proteins. Upon activation, B cells produce antibodies which bind antigens like e.g. molecules from pathogens or vaccines. The drawback of a vast range of different B cell receptors is the potential that some of the receptors recognise self-antigens which can then result in auto-immune disorders. The bone marrow continuously releases immature B cells into the blood stream. A high proportion of these so-called transitional B cells are able to recognise self-antigens via their BCR. It has been unknown where in the body these auto-reactive cells are checked and removed from the circulation. A recent publication by Anna Vossenkämper and Jo Spencer (Kings College) tracked the fate of human transitional B cells and identified that these cells ...
Infection with HIV drives significant alterations in B cell phenotype and function that can markedly influence antibody responses to immunisation. Anti-retroviral therapy (ART) can partially reverse many aspects of B cell dysregulation, however complete normalisation of vaccine responsiveness is not …
Sato S., Miller A.S., Howard M.C., Tedder T.F.. B lymphocyte development and function are regulated in part by the CD19 cell surface receptor complex, which is composed of at least four proteins; CD19, CD21 (CR2, complement receptor 2), CD81, and Leu 13. Because this complex has eight membrane-spanning domains and six cytoplasmic regions, determining the molecular basis for its function and signal transduction activities has not been straightforward. In this study, the contribution of the CD19 cytoplasmic domain to the in vivo function of the CD19/CD21/CD81/Leu 13 complex was assessed by generating CD19-deficient mice that expressed a transgene that encoded only the extracellular and transmembrane domains of CD19. Mice expressing this transgene were similar, if not identical, to CD19-deficient mice with abnormal B cell development, a lack of B-1 cells, increased surface IgM levels on B cells, modest mitogen responses, minimal serum Ig levels, and low humoral immune responses. The results of this ...
TY - JOUR. T1 - How specific is too specific? B-cell responses to viral infections reveal the importance of breadth over depth. AU - Baumgarth, Nicole. PY - 2013/9. Y1 - 2013/9. N2 - Influenza virus infection induces robust and highly protective B-cell responses. Knowledge gained from the analysis of such protective humoral responses can provide important clues for the design of successful vaccines and vaccination approaches and also provides a window into the regulation of fundamental aspects of B-cell responses that may not be at play when responses to non-replicating agents are studied. Here, I review features of the B-cell response to viruses, with emphasis on influenza virus infection, a highly localized infection of respiratory tract epithelial cells, and a response that is directed against a virus that continuously undergoes genetic changes to its surface spike protein, a major target of neutralizing antibodies. Two aspects of the B-cell response to influenza are discussed here, namely ...
In this study we analyzed the effect of CD40 stimulation on the activity and nuclear appearance of Rel/nuclear factor kappaB (NF-kappaB) factors in primary murine B lymphocytes. We show that triggering of CD40 signaling pathway(s) by CD40 ligands expressed on L cells led to strong activation of an NF-kappaB-controlled beta-globin reporter gene in primary B lymphocytes from transgenic mice. Analyses of nuclear translocation of individual members of Rel proteins after CD40 induction of primary B cells showed a strong and long-lasting accumulation of RelB and, less pronounced, of c-Rel. LPS stimulation did not give rise to a persistent nuclear accumulation of RelB and c-Rel, whereas nuclear c-Rel, but not RelB, accumulated after B cell receptor stimulation. CD40 induced not only nuclear translocation but also de novo synthesis of RelB RNA and protein. S107 plasmacytoma cells, which express CD40 but are defective for the nuclear appearance of p50/p65-NF-kappaB, do not express RelB after CD40 stimulation. In
TY - JOUR. T1 - Effects of IL-4 and Fcγ receptor II engagement on Egr-1 expression during stimulation of B lymphocytes by membrane immunoglobulin crosslinking. AU - Klaus, Stephen J.. AU - Phillips, Nancy E.. AU - Parker, David C.. PY - 1993/11. Y1 - 1993/11. N2 - Egr-1 is an immediate early gene that is rapidly upregulated in response to mitogenic signals induced by antigen receptor crosslinking on murine B lymphocytes. It has been shown that levels of Egr-1 expression are closely correlated with B cell proliferation in several models of B cell activation and tolerance. We compared the expression of Egr-1 during B cell stimulation with Fab′2 and IgG anti-immunoglobulin (anti-IG), since it is known that Fab′2 anti-Ig is mitogenic while IgG anti-Ig is not, owing to a dominant inhibitory effect of crosslinking the B cell Fcγ RII to membrane Ig. While mitogenic doses of Fab′2 anti-Ig induce large and rapid increases in Egr-1 expression, IgG anti-Ig results in smaller increases in Egr-1 ...
Most immune cell communication takes place by intercellular transfer of cytokines or the contact-dependent interaction of surface receptors in immunological synapses. In this issue of the European Journal of Immunology, Gardell and Parker (Eur. J. Immunol. 2017, 47, 41-50) point to a new, hybrid mechanism for Th1-cell delivery of help to B cells, based on contact-dependent CD40L transfer. The transfer process and its specificity are both cell contact dependent and antigen dependent. CD40 expression is also required on the B-cell surface to capture the CD40L presented by the Th1 cell. While further studies are needed to confirm the phenomenon in vivo and to test the role of transferred CD40L in other aspects of T-cell help, this study provides an exceptional take-off point and makes excellent use of mouse genetics to work out some possible rules for B cells being able to order help to go.
We show here that approximately 25% of the mature peripheral B cells can survive in the mouse for at least 2 months without Syk, in a manner that requires BAFF‐R and CD19 signaling. In contrast, deletion of the Syk gene in early B cells results in the appearance of a small number of immature IgM+ B cells, which, however, fail to give rise to any mature B cells in the periphery (Cheng et al, 1995). Thus, pre‐B and mature B cells have different requirements for Syk. Indeed, the pre‐BCR is an autonomously signaling receptor that continuously engages Syk, whereas the BCR forms an autoinhibited oligomer on mature B cells that is not in contact with Syk. This notion is supported by a proximity ligation analysis showing that Syk is localized near the BCR only after BCR activation (Infantino et al, 2010; Klasener et al, 2014).. The presence of large amounts of Syk‐negative mature B cells in the induced mb1‐CreERT2;Sykfl/fl mice allowed us to analyze the in vivo role of this kinase in the ...
We show here that approximately 25% of the mature peripheral B cells can survive in the mouse for at least 2 months without Syk, in a manner that requires BAFF‐R and CD19 signaling. In contrast, deletion of the Syk gene in early B cells results in the appearance of a small number of immature IgM+ B cells, which, however, fail to give rise to any mature B cells in the periphery (Cheng et al, 1995). Thus, pre‐B and mature B cells have different requirements for Syk. Indeed, the pre‐BCR is an autonomously signaling receptor that continuously engages Syk, whereas the BCR forms an autoinhibited oligomer on mature B cells that is not in contact with Syk. This notion is supported by a proximity ligation analysis showing that Syk is localized near the BCR only after BCR activation (Infantino et al, 2010; Klasener et al, 2014).. The presence of large amounts of Syk‐negative mature B cells in the induced mb1‐CreERT2;Sykfl/fl mice allowed us to analyze the in vivo role of this kinase in the ...
We have used a novel hu-mouse model expressing a human-specific surrogate self-Ag to formally demonstrate that developing human B cells use receptor editing as a mechanism of central B cell tolerance. Central B cell tolerance in hu-mice is stringent but incomplete. Although the selection of autoreactive B cells into the periphery is rare, variations in the extent of tolerance were observed and shown to depend on the amount of self-Ag as well as the individual genetics of the source of CB.. To date, most studies of human B cell tolerance have focused on limited repertoire analyses of B cell subsets present in peripheral blood (Meffre and Wardemann, 2008; Meffre, 2011). These studies have been invaluable in establishing the presence of tolerance checkpoints, but they have been limited to a poorly defined set of self-Ags without a clear understanding of how these Ags directly affect B cells in vivo. In fact, although a significant reduction in the frequency of autoreactive clones in the human B ...
Redox-regulation of receptors and transcription factors are important for lymphocyte activation, differentiation and apoptosis. Thioredoxin (Trx) is a key redox-regulating protein and oxidative stress sensor operating in synergy with Trx-reductase and protein disulfide isomerase (PDI). The expression of Trx, PDI, and the Trx-regulated transcription-factor Pax5 were analyzed in a panel of human B cell lines and were compared with that of the Bcl-2 family proteins, also redox-controlled. The panel included representative cells from various stages: FLEB14-4 (pro-B), REH and NALM-6 (pre-B), Rael and Daudi (small mature B), U-698 and NC0467.3 (B-blasts), LP-1, U-1996, and U-266 (plasma cells). We found a significant congruence and co-variation of Trx and Bcl-2 levels in the B-lineage, with high expression levels in early stages (pro-B and pre-B) and in the late stage representing terminally-differentiated plasma cells, whereas mid-stage small resting B cells showed a very low expression. PDI ...
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The expression of the CD24 molecule, a glycoprotein expressed at the surface of most B lymphocytes and differentiating neuroblasts, was studied in developing nerve and muscle (after 16 weeks of gestat
Little is know about the nature of peripheral B cell tolerance or how it may vary in distinct lineages. Although autoantibody transgenic studies indicate that anergy and apoptosis are involved, some studies claim that receptor editing occurs. To model peripheral B cell tolerance in a normal, polyclonal immune system, we generated transgenic mice expressing an Igκ-light chain-reactive superantigen targeted to the plasma membrane of hepatocytes (pAlb mice). In contrast to mice expressing κ superantigen ubiquitously, in which κ cells edit efficiently to λ, in pAlb mice, κ B cells underwent clonal deletion. Their κ cells failed to populate lymph nodes, and the remaining splenic κ cells were anergic, arrested at a semi-mature stage without undergoing receptor editing. In the liver, κ cells recognized superantigen, down-regulated surface Ig, and expressed active caspase 3, suggesting ongoing apoptosis at the site of B cell receptor ligand expression. Some, apparently mature, κ B1 and ...
A first clue that SPMs might affect B cell functions was the discovery that B cells express the ALX/FPR2 receptor that recognizes the D-series resolvins, RvD1 and RvD3 (79). 17-HDHA, RvD1, and PD1 are naturally produced within the spleen, a site where B cells commonly reside (35). PUFAs present in omega-3 fatty acid-rich fish oil (precursors for SPM production) were shown to affect B cell functions in mice by increasing antibody production and B cell activation (71, 72, 74). Similarly, mice fed a diet rich in DHA and EPA had a higher number of IgM-expressing splenic B cells following antigen stimulation compared with mice not receiving a PUFA-enriched diet (71). In a mouse model of diet-induced obesity, mice fed a high-fat (Western) diet containing primarily omega-6 fatty acids exhibited diminished antibody titers and increased mortality to influenza challenge relative to a normal diet. These effects could be rescued with dietary DHA (69). Dietary supplementation with PUFAs or PUFA-enriched fish ...
The production of antibody to a thymus-dependent Ag requires cooperation between the B cell and an Ag-specific Th cell. MHC restriction of this interaction implies that the Th cell recognizes Ag on the B cell surface in the context of MHC molecules and that the Ag-specific B cell gets help by acting as an APC for the Th cell. However, a number of studies have suggested that normal resting B cells are ineffective as APC, implying that the B cell must leave the resting state before it can interact specifically with a Th cell. Other studies, including our own with rabbit globulin-specific mouse T cell lines and hybridomas, show that certain T cell lines can be efficiently stimulated by normal resting B cells. One possible explanation for the above contradiction is that our B cells have become activated before presentation. Here we show that presentation by size-selected small B cells is not the result of nonspecific activation signals generated by the T cells or components of the medium. Also, although LPS
Recent in vitro studies have established that activated B cells express OX40 ligand (L), a member of the tumor necrosis factor/nerve growth factor family of cyt
Looking for online definition of pre-B lymphocyte in the Medical Dictionary? pre-B lymphocyte explanation free. What is pre-B lymphocyte? Meaning of pre-B lymphocyte medical term. What does pre-B lymphocyte mean?
The ICOS-B7h costimulatory receptor-ligand pair is required for germinal center formation, the production of isotype-switched antibodies, and antibody affinity maturation in response to T cell-dependent antigens. However, the potentially distinct roles of regulated B7h expression on B cells and dendritic cells in T cell-dependent antibody responses have not been defined. We generated transgenic mice with lineage-restricted B7h expression to assess the cell-type specific roles of B7h expression on B cells and dendritic cells in regulating T cell-dependent antibody responses. Our results show that endogenous B7h expression is reduced on B cells after activation in vitro and is also reduced in vivo on antibody-secreting plasma B cells in comparison to both naïve and germinal center B cells from which they are derived. Increasing the level of B7h expression on activated and plasma B cells in B-B7hTg mice led to an increase in the number of antibody-secreting plasma cells generated after immunization and a
Fingerprint Dive into the research topics of Retinoic acid inhibits IL-6-dependent but not constitutive STAT3 activation in Epstein-Barr virus-immortalized B lymphocytes.. Together they form a unique fingerprint. ...
TY - JOUR. T1 - SIgM-fcmr interactions regulate early b cell activation and plasma cell development after influenza virus infection. AU - Nguyen, Trang T.T.. AU - Graf, Beth A.. AU - Randall, Troy D.. AU - Baumgarth, Nicole. PY - 2017/9/1. Y1 - 2017/9/1. N2 - Previous studies with mice lacking secreted IgM(sIgM) due to a deletion of the ms splice region (ms2/2) had shown sIgM involvement in normal B cell development and in support of maximal Ag-specific IgG responses. Because of the changes to B cell development, it remains unclear to which extent and how sIgM directly affects B cell responses. In this study, we aimed to explore the underlying mechanisms of sIgM-mediated IgG response regulation during influenza virus infection. Generating mice with normally developed ms-deficient B cells, we demonstrate that sIgM supports IgG responses by enhancing early Ag-specific B cell expansion, not by altering B cell development. Lack of FcmR expression on B cells, but not lack of Fca/mR expression or ...
We have studied the role of major histocompatibility complex (MHC) molecules in the regulation of intercellular adhesion of human B cells. We found that molecules able to bind to MHC class II molecules, such as monoclonal antibodies or staphylococcal enterotoxins, induced rapid and sustained homotypic adhesion of Epstein-Barr virus (EBV)-transformed B cell lines as well as peripheral blood B lymphocytes. Moreover, anti-MHC class I monoclonal antibodies also stimulated intercellular adherence. Adhesion induced upon MHC engagement was faster and stronger than that triggered by phorbol esters. It needed active metabolism, but divalent cations were not required. Monoclonal antibodies directed against LFA-1 (CD11a/CD18) or its ligand ICAM-1 (CD54) did not inhibit MHC class II-induced homotypic adhesion of various EBV-transformed B cell lines, nor of a variant of the B cell line Raji expressing very low LFA-1 surface levels. Moreover, EBV-transformed B cells from a severe lymphocyte adhesion deficiency
Altered functional B cell subset populations in patients with chronic fatigue syndrome compared to healthy controls. Bradley AS, et al. Show all...
Rationale: Furthermore to their well-known function as antibody-producing cells, B lymphocytes can markedly influence the course of infectious or noninfectious diseases via antibody-independent mechanisms. response 88) signaling. deficiency correlated with an enhanced accumulation of regulatory/antiinflammatory macrophages in Mtb-infected lungs. Conclusions: Mouse monoclonal to PTK7 Type I IFN produced by Mtb-stimulated B cells favors macrophage polarization toward a regulatory/antiinflammatory phenotype during Mtb contamination. in an innate manner to create type I IFN to eventually modulate the polarization of macrophages toward a regulatory/antiinflammatory profile and in contaminated lungs. This pathway was seen in a murine style of TB and in B cells isolated from sufferers with TB. Our observations reveal B cells as book regulators of immunity to TB through type I IFNCmediated polarization of myeloid cells. Infections with (Mtb) qualified prospects to the forming of lung lesions, the ...
It is generally assumed that chronic lymphocytic leukemia of B cell origin (B-CLL) is characterized by the presence of surface membrane immunoglobulins (SmIg) and by the absence of cytoplasmic immunoglobulins (CyIg). In a variable number of cases SmI
The contribution of intrinsic defects in B and/or T cell function or impaired T-B cell interaction towards poor recall and neo-antigen vaccine responses in HIV-1 infection are not fully understood. Using CVID as a model for B cell maturation, we show patients with untreated HIV-1 infection have increased transitional and tissue like B cells and reduced IgM memory and class switched memory B cell proportions. Loss of IgM memory B cells is associated with progressive HIV-1. Antiretroviral therapy reduces transitional and tissue like B cell percentages but does not restore IgM memory or class switched memory proportions. Most HIV-1 patients on ART have reduced antibody levels post tetanus and pneumococcal vaccination. IgM memory B cell depletion associates with poor post vaccine IgM pneumococcal titres in HIV-1 suggesting loss of IgM memory B cells may be a risk factor for invasive pneumococcal disease. CVID patients with lung disease had lower memory B cells and a trend towards a loss of IgM ...
Lymphadenopathy and lymph node B cell activation are independent of MyD88-signaling.Control C57BL/6 (wildtype) and congenic MyD88−/− mice (n = 6 per gro
Memory B cells are generated in germinal centers (GC) and contribute to serological immunity by rapidly differentiating into plasma cells. Human memory B cells can be identified by the expression of CD27. These cells exhibit more rapid responses than naive (CD27-) B cells following stimulation in vitro, consistent with the heightened kinetics of secondary responses in vivo. CD27+ B cells express mutated Ig V region genes; however a significant proportion continue to express IgM, suggesting the existence of IgM+ memory B cells. The observation that mutated IgM+CD27+ B cells are generated in humans who cannot form GC led to the conclusions that these cells are generated independently of GC and thus are not memory cells and that they mediate responses to T cell-independent Ag. Although some studies support the idea that IgM+CD27+ B cells participate in T cell-independent responses, many others do not. In this review we will provide alternate interpretations of the biology of IgM+CD27+ B cells and propose
We determined that, as compared with human naïve B cells, human GC B cells have a higher intrinsic affinity threshold for antigen. We observed that independently of other extrinsic factors, such as competition among B cells for antigen, the intrinsic affinity of GC B cells for an antigen dictated each subsequent step in B cell activation from the magnitude of BCR signaling to the receptivity of BCR-stimulated GC B cells to Tfh cell signals that drive IRF-4 expression and PC differentiation. We provided evidence that BCRs on LZ GC B cells are concentrated in distinct, highly dynamic, ezrin- and actin-rich pod-like structures through which the BCRs engage antigen, signal, exert pulling forces, and extract antigen from membranes. In contrast, the BCRs on naïve B cells function in flat, stable membrane contacts, with antigen-containing surfaces displaying the well-described features of immune synapses and cSMACs. The role of these pod-like structures in establishing high-affinity thresholds for GC ...
B-cell chronic lymphocytic leukemia (CLL) patients display leukemic clones bearing either germline or somatically mutated immunoglobulin heavy variable (IGHV ) genes. Most information on CLL immunoglobulins (Igs), such as the definition of stereotyped B-cell receptors (BCRs), was derived from germline unmutated Igs. In particular, detailed studies on the distribution and nature of mutations in paired heavy- and light-chain domains of CLL clones bearing mutated Igs are lacking. To address the somatic hyper-mutation dynamics of CLL Igs, we analyzed the mutation pattern of paired IGHV-diversity-joining (IGHV-D-J ) and immunoglobulin kappa/lambda variable-joining (IGK/LV-J ) rearrangements of 193 leukemic clones that displayed ≥ 2% mutations in at least one of the two immunoglobulin variable (IGV ) genes (IGHV and/or IGK/LV ). The relationship between the mutation frequency in IGHV and IGK/LV complementarity determining regions (CDRs) and framework regions (FRs) was evaluated by correlation ...
TY - JOUR. T1 - Expression of the costimulator molecules, CD40 and CD154, on lymphocytes from neonates and young children. AU - Elliott, Salenna. AU - Roberton, Don M.. AU - Zola, Heddy. AU - MacArdle, Peter J.. PY - 2000/1/1. Y1 - 2000/1/1. N2 - Differential expression of the costimulator molecules CD40 and CD154 on neonatal lymphocytes may be one explanation for limited T-dependent antibody responses in human neonates. CD40 was expressed at similar levels on resting B cells from adults, young children (2-20 months of age) or cord blood. CD40 expression was higher on cord blood B cells compared to adult B cells after stimulation with PMA and ionomycin, but similar on adult and cord blood B cells activated by CD3-stimulated T cells. In contrast to previous reports, cord blood T cells stimulated with PMA and ionomycin expressed adult levels of CD154 initially, but this expression was more transient on cord blood T cells. When adult and cord blood mononuclear cells were stimulated with CD3 mAb, T ...
Cancer immunotherapy by therapeutic activation of T cells has demonstrated clinical potential. Approaches include checkpoint inhibitors and chimeric antigen receptor T cells. Here, we report the development of an alternative strategy for cellular immunotherapy that combines induction of a tumor-directed T-cell response and antibody secretion without the need for genetic engineering. CD40 ligand stimulation of murine tumor antigen-specific B cells, isolated by antigen-biotin tetramers, resulted in the development of an antigen-presenting phenotype and the induction of a tumor antigen-specific T-cell response. Differentiation of antigen-specific B cells into antibody-secreting plasma cells was achieved by stimulation with IL21, IL4, anti-CD40, and the specific antigen. Combined treatment of tumor-bearing mice with antigen-specific CD40-activated B cells and antigen-specific plasma cells induced a therapeutic antitumor immune response resulting in remission of established tumors. Human CEA or ...
The integrin LFA-1 and its ligand ICAM-1 mediate B cell adhesion, but their role in membrane-bound antigen recognition is still unknown. Here, using planar lipid bilayers and cells expressing ICAM-1 fused to green fluorescence protein, we found that the engagement of B cell receptor (BCR) promotes B cell adhesion by an LFA-1-mediated mechanism. LFA-1 is recruited to form a mature B cell synapse segregating into a ring around the BCR. This distribution is maintained over a wide range of BCR/antigen affinities (10(6) M(-1) to 10(11) M(-1)). Furthermore, the LFA-1 binding to ICAM-1 reduces the level of antigen required to form the synapse and trigger a B cell. Thus, LFA-1/ICAM-1 interaction lowers the threshold for B cell activation by promoting B cell adhesion and synapse formation.
TY - JOUR. T1 - Cytoplasmic IgM in leukemic B cells by flow cytometry. AU - Loftin, Karin C.. AU - Reuben, James M.. AU - Hersh, Evan M.. AU - Sujansky, Daniel. PY - 1985. Y1 - 1985. N2 - The presence of intracellular cytoplasmic immunoglobulin M (IgM) in leukemic cells from patients with acute lymphocytic leukemia (ALL) and chronic lymphocytic leukemia (CLL) was investigated by flow cytometry. The objective of the study was to develop a reproducible flow cytometric method. A Burkitts lymphoma-derived B-cell line, Daudi, and a pre-B ALL, Nalm-6, served as prototypes. Normal B cells and cells from patients with chronic myelogenous leukemia (CML) were used as negative controls. Cytoplasmic μ was expressed in 77.3 ± 7.5% (n = 10) of Nalm-6 cells. CALLA+ ALL and CML cells lacked cytoplasmic μ. The surface-membrane immunoglobulin on the viable B cells was blocked with purified goat anti-human IgM. Subsequently, the B cells were fixed in cold absolute methanol and stained with a ...
Exosomes are lipid bound nanovesicles that are formed via the inward budding of the endosomal membrane, then released upon fusion of the endosomal limiting membrane with the plasma membrane. The majority of exosome studies involve the use of exosomes from bone marrow-derived dendritic cells or immortalised cell lines. This research project has focused on exosomes derived from primary B cells in response to T cell signalling, in particular via the CD40 and the interleukin-4 receptors. The fate of exosomes following their release is largely unknown. However as we have previously identified that B cell-derived exosomes are enriched in the antigen presenting molecules major histocompatibility complex class I (MHC-I), MHC-II and immunoglobulin, this may implicate B cell-derived exosomes in the transfer of antigen. We have sought to address the physiological role of primary B cell-derived exosomes and their interactions with other cells within secondary lymphoid tissue in vivo. We identified ...
As we know, antibodies are used extensively in diagnostics and as therapeutic agents. Achieving high-affinity binding is crucial for expanding detection limits, extending dissociation half-times, decreasing drug dosages and increasing drug efficacy. In order to conquer the shortages of common antibodies, Creative Biolabs developed antibody affinity maturation service.. Weve gained extensive experience in antibody affinity maturation over the years. We use scFv as the antibody format and monovalent display phagemid as the system to reduce the avidity effects during antigen-binding screening, said Dr. Monica Müller, chief scientific officer of Creative Biolabs.. As Dr. Monica introduced, untargeted mutagenesis and oligonucleotide-directed mutagenesis are used to construct random or defined sub-libraries to introduce a large number of mutants of the original antibody. Antibody binders of higher affinity are then selected by increasing the screening stringency. By constructing a series of ...
As we know, antibodies are used extensively in diagnostics and as therapeutic agents. Achieving high-affinity binding is crucial for expanding detection limits, extending dissociation half-times, decreasing drug dosages and increasing drug efficacy. In order to conquer the shortages of common antibodies, Creative Biolabs developed antibody affinity maturation service.. Weve gained extensive experience in antibody affinity maturation over the years. We use scFv as the antibody format and monovalent display phagemid as the system to reduce the avidity effects during antigen-binding screening, said Dr. Monica Müller, chief scientific officer of Creative Biolabs.. As Dr. Monica introduced, untargeted mutagenesis and oligonucleotide-directed mutagenesis are used to construct random or defined sub-libraries to introduce a large number of mutants of the original antibody. Antibody binders of higher affinity are then selected by increasing the screening stringency. By constructing a series of ...
B1 cells are a sub-class of B cell lymphocytes that are involved in the humoral immune response. They are not part of the adaptive immune system, as they have no memory, but otherwise, B1 cells perform many of the same roles as other B cells: making antibodies against antigens and acting as antigen presenting cells. Notably, most B1 cells do not develop into memory B cells. B1b cells have been shown to be capable of memory responses. See B1b lymphocytes confer T cell-independent long-lasting immunity. B1 cells are first produced in the fetus and most B1 cells undergo self-renewal in the periphery, unlike conventional B cells (B2 cells) that are produced after birth and replaced in the bone marrow. In January 2011, human B1 cells were found to have marker profile of CD20+CD27+CD43+CD70- and could either be CD5+ or CD5-, which has been debated since. CD5-CD72 is thought to mediate B cell-B cell interaction. B-1 B cells, in the mouse, can be further subdivided into B-1a (CD5+) and B-1b (CD5−) ...
TY - JOUR. T1 - Aged mice exhibit distinct B cell precursor phenotypes differing in activation, proliferation and apoptosis. AU - Van der Put, Elaine. AU - Sherwood, Erin M.. AU - Blomberg, Bonnie B. AU - Riley, Richard L. PY - 2003/10/1. Y1 - 2003/10/1. N2 - Senescence in murine models is associated with a reduction, albeit heterogeneous, in bone marrow pre-B cells. We have categorized aged BALB/c mice into two phenotypes based on their patterns of pre-B/pro-B cell loss. Each phenotype is characterized by distinct responses to the growth cytokine IL-7 and capacity for survival in vitro. A moderate loss of late-stage pre-B cells (25-80%) coincided with decline in proliferation to rmIL-7. This was also associated with a decrease in the frequency of pro-B cells which increased phosphotyrosine content upon IL-7 stimulation, an indicator of early activation events. A severe loss of pre-B cells (,80%) resulted in a reduced pro-B cell pool which retained normal activation and proliferative ...
Differentiation of tumor B lymphocytes. The team also studies the genetic and epigenetic modifications of tumor B cells in follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL). In FL, we identified a phospho-STAT3 (pSTAT3) hyper-signaling correlated with an increase of IL-21 secretion by Tfh and with the expression of some target genes of pSTAT3. However the key gene of the B cell differentiation into plasma cell, PRDM1, a pSTAT3 target gene of, has a weak expression in FL, highlighting the existence of genetic and epigenetic abnormalities related to the disease. We aim to understand these deregulations, in particular by showing the importance of the acetylation properties in the B differentiation and in the control of the PRDM1 gene expression. Our work supports clinicians in their choice to use new therapeutics targeting the epigenome, such as the histone acetyltransferase inhibitors (HDACi), in treating FL patients.. As for the technology employed, we implemented a gene capture ...
While B cells are traditionally regarded as marketers of the immune system response via antibody release and pro-inflammatory cytokine creation, latest research have got verified an essential function for B-cell-mediated detrimental regulations of immunity also. in the full years to follow. The past 10 years provides noticed remarkable developments in our understanding of B-cell immunoregulation. Mizoguchi advancement of this exclusive regulatory people. Nevertheless, the identity of IL-10-making resistant cells is normally barely a simple job and continues to be complicated in the field of regulatory B-cell biology (18). This is normally because specific spleen C cells singled out from unsuspecting wildtype rodents perform not really constitutively sole or secrete measurable IL-10 proteins without account activation. Provided the incapacity to observe C10 cells straight assays to detect cytokine creation in Testosterone levels cells had been improved to recognize C cells that had been ...
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Learn how you can enhance your experiment and upgrade your B cell culture with this webinar. We will share insights into how you can optimize and standardize your B cell culture in experimental studies. | Lëtzebuerg
Learn how you can enhance your experiment and upgrade your B cell culture with this webinar. We will share insights into how you can optimize and standardize your B cell culture in experimental studies. | France
article{9a5c9918-f28d-42f7-9e4a-e617d47af020, abstract = {Development of type-II collagen (CII)-induced arthritis (CIA) is dependent on a T-cell mediated activation of autoreactive B cells. However, it is still unclear if B cells can present CII to T cells. To investigate the role of B cells as antigen-presenting cells (APCs) for CII, we purified B cells from lymph nodes of immunized and nonimmunized mice. These B cells were used as APC for antigen-specific T-cell hybridomas. B cells from naïve mice did present native, triple-helical, CII (nCII) but also ovalbumin (OVA) and denatured CII (dCII) to antigen-specific T-cell hybridomas. In addition, B cells primed with nCII or OVA, but not dCII, activated the antigen-specific T-cell hybridomas two to three times better than naïve B cells. We conclude that antigen-primed B cells have the capacity to process and present CII to primed T cells, and antigen-primed antigen-specific B cells are more efficient as APC than naïve B cells. We further ...
Secretory IgA (S-IgA) is a hallmark antibody principally produced at mucosal sites and plays an important role in the creation of immunological surveillance and homeostasis at mucosa. In addition to the IgA induction through gut-associated lymphoid tissues (e.g., Peyers patch), peritoneal B cells have been considered to be another source of S-IgA, especially specific for the T-independent antigen. Here we show that the trafficking of peritoneal B cells is principally regulated by sphingosine 1-phosphate (S1P). Peritoneal B cells expressed high levels of the type 1 S1P receptor. Thus, disruption of S1P-mediated signaling caused a rapid disappearance of peritoneal B cells. These changes did not affect natural plasma antibody production or phosphorylcholine (PC)-specific antibody production in serum after peritoneal immunization with heat-killed streptococcal pneumoniae. However, it dramatically reduced peritoneal B cell-derived natural intestinal S-IgA production without affecting the expression ...
TY - JOUR. T1 - Inhibition of EBV-induced lymphoproliferation by CD4+ T cells specific for an MHC class II promiscuous epitope. AU - Omiya, Ryusuke. AU - Buteau, Chantal. AU - Kobayashi, Hiroya. AU - Paya, Carlos V.. AU - Celis, Esteban. PY - 2002/8/15. Y1 - 2002/8/15. N2 - Posttransplant lymphoproliferative disorder (PTLD) and B cell lymphomas induced by EBV continue to be a major life-threatening complication in transplant patients. The establishment and enhancement of T cell immunity to EBV before transplantation and immunosuppressive therapy could help diminish these complications, but the lack of an effective vaccine has limited this prophylactic approach. We describe here the identification of a peptide epitope from the EBV EBNA2 Ag that is capable of inducing in vitro CD4+ T cell responses that inhibit the EBV-mediated B lymphocyte proliferation associated with PTLD. Most significantly, T cell responses to the EBNA2 epitope were found to be restricted by numerous MHC class II alleles ...
Ittigen, Switzerland (ots) - Pevion Biotech AG today announced further data from the ongoing clinical study of its therapeutic Candida vaccine PEV7, demonstrating the generation...
B-cell growth factor 1, 12kDa, also known as BCGF1, is a human gene. B-cell growth factor is released by T lymphocytes after either lectin or antigen stimulation. It supports the clonal proliferation of B lymphocytes. Entrez Gene: BCGF1 B-cell growth factor 1, 12kDa. Kumar A, Vasquez A, Maizel AL, Sharma S (1991). Human BCGF-12kD functions as an autocrine growth factor in transformed B cells. European Cytokine Network. 1 (2): 109-13. PMID 1966378. Vazquez A, Mills S, Sharma S, Maizel AL (October 1988). Expression of CD23 antigen is not necessary for human 12-kDa B cell growth factor-mediated B cell proliferation. European Journal of Immunology. 18 (10): 1647-9. doi:10.1002/eji.1830181029. PMID 2973416. Mehta SR, Sandler RS, Ford RJ, Sharma S, Maizel AL (1986). Cellular interaction between B and T lymphocytes: enhanced release of B cell growth factor. Lymphokine Research. 5 (1): 49-57. PMID 3484798. Ennist DL, Greenblatt D, Coffman R, Sharma S, Maizel A, Howard M (November 1987). ...
Inversion of CD4(+)/CD8(+) ratio in B chronic lymphocytic leukemia correlates with differential sensitivity of CD4(+) and CD8(+) T lymphocytes to the killing efficacy of Fas (APO-1/CD95) ligand(+) tumor cells ...
Chronic lymphocytic leukemia (CLL) is a clonal disease of B lymphocytes manifesting as an absolute lymphocytosis in the blood. However, not all lymphocytoses are leukemic. In addition, first-degree relatives of CLL patients have an ~15 % chance of developing a precursor condition to CLL termed monoclonal B cell lymphocytosis (MBL), and distinguishing CLL and MBL B lymphocytes from normal B cell expansions can be a challenge. Therefore, we selected FMOD, CKAP4, PIK3C2B, LEF1, PFTK1, BCL-2, and GPM6a from a set of genes significantly differentially expressed in microarray analyses that compared CLL cells with normal B lymphocytes and used these to determine whether we could discriminate CLL and MBL cells from B cells of healthy controls. Analysis with receiver operating characteristics and Bayesian relevance determination demonstrated good concordance with all panel genes. Using a random forest classifier, the seven-gene panel reliably distinguished normal polyclonal B cell populations from expression